Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1978-1-27
pubmed:abstractText
The influence of steroid hormones on the response of human astrocytoma cells (1321N1) to prostaglandin E(1) (PGE(1)) has been investigated. Responsiveness to PGE(1) was determined by measuring the conversion of [(3)H]ATP to cyclic [(3)H]AMP in cells prelabeled with [(3)H]adenine. After incubation of the cells with dexamethasone, a marked increase in both the maximal effect (2- to 3-fold) and the potency (5-fold) of PGE(1) was observed. The effect was specific for the action of PGE(1) in that no change in the response of the cells to isoproterenol was observed. The EC(50) for dexamethasone was 0.001 muM and the effect was dependent on the presence of serum. The effect of dexamethasone was first observed after a 30- to 60-min lag and was maximal by 6-8 hr. Preconfluent cultures (3 days after seeding) exhibited optimal responsiveness to glucocorticoids. Both hydrocortisone and corticosterone mimicked the effect of dexamethasone but both were less potent. The action of dexamethasone was blocked by progesterone, testosterone, and 17alpha-methyltestosterone. Cycloheximide, at a concentration (1.0 mug/ml) that blocked protein synthesis (>90%) in 1321N1 cells, totally prevented the effect of dexamethasone on the response of the cells to PGE(1). Upon removal of dexamethasone from cells treated for 16 hr, responsiveness to PGE(1) returned to control levels with a half-time of 4 hr. Dexamethasone also was found to increase the response to PGE(1) of a Rous sarcoma virus-transformed human astrocytoma cell line and the WI-38 human fibroblast line. The most obvious interpretation of our findings is that glucocorticoids induce the synthesis of a protein that selectively modifies the sensitivity of adenylate cyclase to PGE(1).
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-1064044, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-1178912, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-14907713, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-163980, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-165356, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-171589, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-176920, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-177468, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-184125, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-184126, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-189229, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-190234, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-191127, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-4150434, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-4313504, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-4314281, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-4337530, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-4365853, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-4369127, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-4369972, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-4376959, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-4395012, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-4399619, http://linkedlifedata.com/resource/pubmed/commentcorrection/200933-4827395
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0027-8424
pubmed:author
pubmed:issnType
Print
pubmed:volume
74
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4816-20
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1977
pubmed:articleTitle
Glucocorticoids increase the responsiveness of cells in culture to prostaglandin E1.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.